An understanding of the role of UVB-induced modulation of chemically-induced skin tumorigenesis would add to our knowledge of host factors in carcinogenesis and could aid in terms of prevention and treatment of malignancy. UVB-induced immuno-suppression is critical for the development of UVB-induced skin tumors, and it is important to kniw if it can influence skin carcinogenesis mediated by other agents. The mouse skin model of chemically induced tumorigenesis will be used in these studies. The kinetics of tumor formation by a number of chemical carcinogens and of UVB-mediated immunosuppression have been delineated in this model. BALB/c, C3H/HeN, and CDF 1 mice will be UVB-irradiated dorsally to induce immunosuppression. After suppression is achieved, the BALB/c mice will be treated with benzo(a)pyrene (BP) in a single stage protocol. Tumor formation in immunosuppressed mice will be compared with that in normal controls. A known carcinogenic dose, plus a 10-fold higher one will be used in the experiments because there is evidence that higher doses of chemical carcinogens yield tumors with higher antigenicity. The immunosuppressed C3H/HeN mice will receive an initiation-promotion regimen, consisting of 7,12-dimethylbenz(a)anthracene and 12-0-tetradecanoylphorbol-13-acetate. Again, tumorigenesis will be compared in immunosuppressed and normal mice. If immunosuppression enhances two stage carcinogenesis, we shall determine whether initiation, promotion, or both are enhanced. The CDF1, (BALB/c x DBA/2) mice, which are pigmented, will be tested for the induction of UVB-mediated immunosuppression and for UV modulation of tumorigenesis mediated by DMBA and TPA. Because this strain has recently been reported to yield melanomas, this study of the role of UVB irradiation effects on chemical induction of tumors in CDF1 may be especially important. We shall also determine if passive transfer of lymphoid cells from UV-suppressed mice are able to prevent growth of antigenic, chemically-induced syngeneic tumors in syngeneic hosts. Additionally, we shall determine if the subpopulation of splenic lymphocytes which displays the Lyt-1 antigens are the mediators of UVB enhancement of chemically induced tumors, as has been demostrated for UV-induced tumors. These experiments will elucidate the potential role of UV irradiation in the modulation of chemical carcinogenesis.